CAQ-Nephrology cheat sheet

Nephritic syndrome: hematuria with dysmorphic RBCs or RBC casts, hypertension, oliguria, and variable proteinuria; nephrotic syndrome: proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia.

IgA nephropathy is the most common primary glomerulonephritis; mesangial IgA deposits, normal complement, and recurrent hematuria after mucosal infection; ACE inhibitor or ARB is first-line antiproteinuric therapy.

Minimal change disease: normal light microscopy, effaced podocyte foot processes, selective proteinuria, and steroid responsiveness; it is the most common childhood nephrotic syndrome.

Focal segmental glomerulosclerosis: segmental sclerosis on light microscopy, nephrotic proteinuria, steroid resistance, and associations with HIV, APOL1 variants, obesity, and heroin use.

Membranous nephropathy: subepithelial deposits, anti-PLA2R antibody in primary disease, and nephrotic syndrome; secondary causes include malignancy, hepatitis B, and drugs; venous thrombosis risk is increased.

Pauci-immune crescentic GN: little immunoglobulin on immunofluorescence, ANCA positivity, and pulmonary-renal syndrome; induction is cyclophosphamide or rituximab plus glucocorticoids.

Anti-GBM disease: linear IgG along the basement membrane and crescentic GN; pulmonary hemorrhage defines Goodpasture syndrome; treatment is plasmapheresis plus cyclophosphamide and glucocorticoids.

Acute interstitial nephritis: culprit drugs include NSAIDs, proton-pump inhibitors, and antibiotics; sterile pyuria, WBC casts, and eosinophiluria may occur; drug withdrawal is the key step.

Chronic tubulointerstitial nephropathy: causes include analgesic nephropathy, lithium, reflux, and obstruction; tubular dysfunction and non-specific casts predominate rather than glomerular hematuria.

Hyponatremia algorithm: confirm hypotonicity by serum osmolality; check urine osmolality and urine sodium; urine osmolality <100 mOsm/kg suggests water intake or low solute; urine sodium <30 mmol/L suggests hypovolemia.

SIADH: euvolemic hypotonic hyponatremia, urine osmolality >100 mOsm/kg, urine sodium >30 mmol/L, normal thyroid and adrenal function; first-line therapy is fluid restriction; correct sodium ≤8 mmol/L in 24 h.

Hyperkalemia ECG: peaked T waves, PR prolongation, widened QRS; give calcium gluconate for membrane stabilization, insulin plus glucose or beta-agonist for shift, and potassium binders or dialysis for removal.

Metabolic acidosis: anion gap = Na − (Cl + HCO3), normal 8–12 mmol/L; high-gap causes include ketoacidosis, lactate, renal failure, and toxins; normal-gap causes include diarrhea and renal tubular acidosis.

Winter formula: expected PaCO2 = 1.5 × HCO3 + 8 ± 2; if measured PaCO2 is higher, concomitant respiratory acidosis; if lower, concomitant respiratory alkalosis.

Renal tubular acidosis: type 1 distal has urine pH >5.5 and stones; type 2 proximal has bicarbonaturia and Fanconi syndrome; type 4 has hyperkalemia from hypoaldosteronism or aldosterone resistance.

Metabolic alkalosis: urine chloride <20 mmol/L suggests saline-responsive vomiting or diuretic use; urine chloride >20 mmol/L suggests saline-resistant mineralocorticoid excess or severe hypokalemia.

Hypokalemia: ECG shows flattened T waves, U waves, and arrhythmias; each 1 mmol/L fall reflects a larger total-body deficit; correct magnesium deficiency to enable potassium repletion.

Hypernatremia: water deficit = total body water × (Na/140 − 1); correct chronic hypernatremia by ≤10 mmol/L/day; free-water deficit is replaced with enteral water or hypotonic intravenous fluid.

KDIGO AKI definition: serum creatinine rise ≥0.3 mg/dL within 48 h, ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/h for 6 h.

Prerenal vs intrinsic AKI: fractional excretion of sodium <1% suggests prerenal; >2% suggests acute tubular necrosis; fractional excretion of urea <35% suggests prerenal when diuretics are used; muddy brown casts indicate ATN.

Urgent renal replacement therapy indications: refractory acidosis, electrolyte disturbance such as severe hyperkalemia, toxic ingestion, volume overload, and uremic complications such as encephalopathy or pericarditis.

Rhabdomyolysis: elevated creatine kinase, positive urine dipstick for blood without red blood cells, hyperkalemia, hypocalcemia, and hyperphosphatemia; treatment is aggressive isotonic fluid resuscitation.

Contrast-associated AKI: risk factors include CKD, diabetes, volume depletion, and high contrast volume; use the lowest necessary contrast volume and isotonic intravenous fluids; routine bicarbonate or N-acetylcysteine is not proven.

CRRT vs intermittent hemodialysis: continuous renal replacement therapy provides gradual solute and fluid removal and is often chosen for hemodynamically unstable patients; trials show no clear mortality benefit over intermittent dialysis.

Abdominal compartment syndrome: bladder pressure >20 mm Hg with new organ dysfunction; treatment is decompression, often surgical, and renal replacement may be needed for associated AKI.

Plasmapheresis is first-line in TTP and anti-GBM disease and is used as adjunctive therapy in severe ANCA vasculitis with pulmonary hemorrhage or rapidly progressive renal failure.

CKD definition: glomerular filtration rate <60 mL/min/1.73 m2 or kidney damage persisting >3 months; stage by GFR category G1–G5 and albuminuria category A1–A3.

CKD anemia: normocytic normochromic anemia; correct iron deficiency first, then consider an erythropoiesis-stimulating agent; target hemoglobin rather than normalizing it.

CKD-MBD: hyperphosphatemia, hypocalcemia, and elevated PTH; treat with dietary phosphate restriction, phosphate binders, and active vitamin D when indicated; avoid calcium overload.

RAAS blockade: ACE inhibitor or ARB reduces proteinuria and progression in albuminuric CKD; check creatinine and potassium after initiation; a creatinine rise up to 30% may be acceptable.

Dialysis initiation: urgent indications include refractory hyperkalemia, acidosis, volume overload, uremic encephalopathy, pericarditis, and bleeding; initiation is based on symptoms and complications, not GFR alone.

Hemodialysis adequacy: thrice-weekly target single-pool Kt/V ≥1.2 and urea reduction ratio >65%; arteriovenous fistula is preferred access because of lower infection and thrombosis rates than catheters.

Peritoneal dialysis peritonitis: cloudy effluent and abdominal pain; diagnosis requires effluent cell count and culture; treatment usually uses intraperitoneal antibiotics and catheter care review.

Kidney transplant: maintenance immunosuppression commonly includes tacrolimus, mycophenolate, and glucocorticoids; rejection may be cellular or antibody-mediated; BK viremia requires reduction of immunosuppression.

Resistant hypertension: blood pressure above goal on 3 agents including a diuretic, or controlled on 4 agents; screen for adherence, white-coat effect, obstructive sleep apnea, primary aldosteronism, and renal artery stenosis.

Primary aldosteronism: screen with plasma aldosterone-to-renin ratio in resistant hypertension, hypokalemia, or adrenal incidentaloma; confirm with saline suppression or captopril testing before adrenal imaging.

Renal artery stenosis: clues include resistant hypertension, flash pulmonary edema, abdominal bruit, and acute kidney injury after starting an ACE inhibitor or ARB; fibromuscular dysplasia affects young women.

Scleroderma renal crisis: malignant hypertension, acute kidney injury, and microangiopathic hemolysis in systemic sclerosis; ACE inhibitors are the cornerstone and should not be withheld.

Thrombotic microangiopathy: microangiopathic hemolytic anemia, thrombocytopenia, and organ injury such as AKI; TTP has ADAMTS13 activity <10% and requires plasma exchange; atypical HUS may respond to eculizumab.

Lupus nephritis: proliferative ISN/RPS class III or IV disease is treated with glucocorticoids plus mycophenolate mofetil or cyclophosphamide; adding a biologic may be considered in selected severe cases.

Diabetic kidney disease: persistent albuminuria and declining GFR; ACE inhibitor or ARB and SGLT2 inhibitor are kidney-protective in appropriate patients; Kimmelstiel-Wilson nodules are a histologic clue.

Hepatorenal syndrome: functional renal failure in advanced liver disease with ascites; terlipressin plus albumin is standard treatment; liver transplantation is definitive; exclude volume depletion, infection, and obstruction first.